Electrical stimulation of body tissue and organs is often used as a method of treating various pathological conditions. Such stimulation generally entails making an electrical contact between body tissue and an electrical pulse generator through use of one or more stimulation leads. Various lead structures and various techniques for implanting these lead structures into body tissue and particularly the heart have been developed.
For example, a transvenous endocardial lead establishes electrical contact between an electrical pulse generator and heart through placement of a lead in the venous system. Specifically, an electrical lead is passed through a vein, with the assistance of a fluoroscope, into the heart where it is held in contact with the endocardium by the trabeculae of the heart chamber, such as the ventricle.
There are, however, disadvantages to this type of lead, including: possible damage to the vein, such as perforation or laceration during insertion; possible failure to securely attach and maintain electrical contact with the heart; possible perforation of the heart wall by the lead; and because direct visual inspection of the lead placement is not possible, possible improper lead placement in the heart.
Besides these possible problems, there are additional situations in which the installation of a transvenous endocardial pacing lead is either not feasible or not recommended. These situations include the case when the vein which would be used is damaged or too small, or the situation in which a physical or anatomical anomaly prevents the placement of a transvenous endocardial lead within the heart, such as the presence of an artificial heart valve.
In particular a transvenous endocardial lead is often either not feasible or recommended in children. One problem presented by use of a transvenous endocardial lead stems from the growth a child undergoes. Specifically, upon chronic implantation of a transvenous lead the lead body is subject to fibrotic encapsulation within the venous system. This encapsulation fixes the lead body in place, especially relative to the walls of the venous system. Over time, as the child grows the venous system elongates. Because the lead is fixed by fibrotic growth, as the venous system elongates the lead electrode will be pulled or dislodged from effective contact with the endocardium. In addition, because the venous system of a child is smaller than an adult, it is less tolerant of the partial occluding of a vein by a transvenous lead. In these cases use of an myocardial lead applied from the epicardium is often indicated or preferred.
A myocardial lead offers a significant advantage to a transvenous endocardial lead with regards to children. Because a myocardial lead is attached to the heart not through the venous system but rather through a thoracic access, a sufficient amount of spare lead length to accommodate growth may be located or looped within the thoracic cavity. In addition a myocardial lead does not even partially occlude a part of the relatively small venous system of a child.
A number of different myocardial leads have been developed, as have various techniques for implanting them within the myocardial tissue of the heart. Typically, myocardial leads are attached from the exterior of the heart through a thoracic access.
One form of such lead is a screw-in lead. This lead consists of a rigid helical coil which is used to fix the electrode to the myocardial tissue. Examples of such a lead may be found in U.S. Pat. No. 5,154,183 to Kreyenhagen et al., U.S. Pat. No. 5,143,090 to Dutcher et al., U.S. Pat. No. 5,085,218 to Heil Jr. et al., and U.S. Pat. No. 4,010,758 to Rockland et al. One problem which has been found to exist with such leads, however, is the inflammatory tissue reaction (or foreign body response) of the tissue to the device and especially the rigid helix. Inflammatory tissue reaction is caused, in part, from the presence of a foreign object within the tissue. It has been found that the presence of a rigid structure within the myocardium chronically creates at least some of the immediately surrounding myocardial tissue to be replaced with either fat or collagen or both. Such tissue reaction detrimentally affects the electrical properties of the surrounding tissue, and thus the lead performance.
One means of treating the inflammatory response has been to provide a means for delivering a drug near the electrode to mitigate the inflammatory tissue reaction described above. Specifically it has been found eluting an anti-inflammatory agent, such as a glucocortico steroid, minimizes tissue irritation, helps reduce or eliminate threshold peaking and further assists in maintaining low acute and chronic pacing thresholds.
In addition a tissue reaction due to the mechanical motion of the cardiac tissue relative to the helical coil has been found to arise in the surrounding tissue. Because the heart is a constantly moving organ, the presence of a stationary and stiff fixation coil exacerbates the normal build-up of collagen and fat near the helical coil. Such tissues may detrimentally affect the electrical performance of the surrounding tissue. As a result stimulation thresholds may rise. As such, a chronic lead which mitigates such tissue reactions would be of benefit.
Maintenance of stimulation thresholds is an important criterion for a chronically implanted cardiac lead. Implantable pulse generators are powered by a battery having a limited life. After an extended period of time, such as five years, the battery will be depleted and the implanted pulse generator must be surgically replaced. Therefore, it is an objective to minimize the electrical current drain on the power source by appropriate design of the pacemaker's electrodes and to provide for reduced stimulation voltage.